Plasticity in the visual cortex is demonstrated in the whole animal by ocular dominance shifts that occur after monocular deprivation. It can also be demonstrated in the form of long-term potentiation (LTP) and long-term depression (LTD). Even though ocular dominance plasticity takes days to occur, and involves anatomical changes, and LTP and LTD are physiological changes produced in minutes, the initial steps in both forms of plasticity are same. For example, both depend in part on the activation of NMDA receptors.These initial steps can be studied with LTP and LTD much more quickly than they can be studied in the intact animal. Moreover, using whole cell recordings, one can study intracortical plasticity and distinguish presynaptic mechanisms from postsynaptic mechanisms, both of which are difficult to do in the intact animal. Both ocular dominance plasticity and LTP have a critical period that varies with age and layer in the visual cortex. We will pursue the hypothesis that there are different mechanisms in different layers and maybe at different ages that account for these variations. NMDA receptors and metabotropic glutamate receptors are both known to be involved in plasticity. Based on our previous work, we suggest that NMDA receptors are important late in the critical period in the upper layers II and III, but not in the lower layers V and VI. Based on our current work, we suggest that Group I metabotropic glutamate receptors play a potentiating role in lower layers, while Group II metabotropic glutamate receptors play a depressive role in upper layers. The second messenger cAMP is increased by metabotropic glutamate receptors by a quantity that is closely related to the critical period. We therefore also suggest that cAMP plays a long-term potentiating role, and based on our current work, that cGMP plays a depressive role.